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Physiology & Science: Neuroscience I > Cell to Cell Communication > Flashcards

Flashcards in Cell to Cell Communication Deck (21)
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1

How do skeletal muscle fibres contract and relax?

Contract when Ach is released at neuromuscular junction

Relax when the alpha-motor neurone itself is inhibited as skeletal muscle fibres only receive one input directly (Ach)

2

What factors increase the speed of AP propagation?

- Larger axon diameter
- More myelinated axon

3

What is the neuro pathology of Multiple Sclerosis?

- LOSS of MYELIN
- Plaques occur anywhere in CNS white matter
- Slows, delays or blocks AP transmission
- producing sensory, motor, cognitive or behavioural deficits

4

Describe the two synapse types

- Electrical
--> cardiac function (gap junctions), present in NS, unclear role

- Chemical
--> majority, many roles using many NTs, therapeutically VERY relevant

5

What are the 4 steps in terms of the life of a neurotransmitter?

1. Synthesis
2. Release
3. Action
4. Removal

6

Describe the 2 types of NT synthesis and therapeutic relevance

1. Synthesis in the cell body (eg. neuropeptides)
2. Local synthesis (eg. catecholamines) (tyr -> l-dopa -> dopamine, NA)

eg. Parkinson's - L-DOPA enzyme increased to produce more dopamine
(dopamine involved in mood, memory, movement, attention etc)

7

Describe NT release and therapeutic relevance

- action potential arrives at terminal bouton
- activates VGCCs
- no calcium inside cell, high outside cell so Ca INFLUX
- Calcium binds to vSNARE + tSNARE proteins
- triggers fusion, exocytosis

eg. Botulinum toxin blocks neuromuscular transmission by interfering with Calcium release

8

What are some features of post-synaptic receptors?

1) excitatory or inhibitory
2) fast (ligand gated/iono) or slow (g protein/metabo)

9

Example and response of ionotropic EXCITATORY receptor

- glutamate in CNS
- Ach @ NMJ

- bind to receptor, cause SODIUM influx -> depolarisation -> EPSP (electrotonic)

10

Example and response of ionotropic INHIBITORY receptor

- GABA
- glycine (spinal cord, retina)

- bind to receptor, cause CHLORIDE influx -> hyperpolarisation -> IPSP (electrotonic)

11

Example and response of metabotropic receptor

- dopamine, ACh, serotonin, NA

- long lasting, involve second messengers, used in MODULATORY pathways

12

Examples of therapeutic interventions in regards to receptor action?

- Some drugs bind to same site as NT
---> nicotine at ionotropic nicotinic Ach receptors
---> curare blocks neuromuscular Ach receptors

- Some drugs bind to other sites on receptor, to modify response to NT
---> benzodiazepines enhance effect of GABA at GABA receptors
---> strychnine reduces effect of glycine at glycine receptors

13

Discuss types and examples of neurotransmitter removal

1) DIFFUSION - peptides

2) ENYMATIC degradation - AChE (inhibitors of this will inc cholinergic transmission)

3) RE-UPTAKE - dopamine, NA, serotonin

4) GLIAL UPTAKE - glutamate, GABA (by astrocytes - for fast transmitters)

14

What is the action of cocaine?

Blocks re-uptake of dopamine into pre-synaptic membrane, resulting in a greater 'reward' feeling.

15

How is hypoxia linked to glutamatergic toxicity?

- uptake of glutamate requires oxygen
- in hypoxic conditions (eg stroke), glutamate remains in the cleft
- toxic effect as it builds up

16

Discuss the negative feedback displayed during synaptic transmission

- presynaptic receptors bind NT released by cell, reduce amount of NT released with each AP, tones things down - site for drugs

- post synaptic receptors send RETROGRADE signals to decrease NT release

17

What's a gr8 saying by P.Murphz?

cells that fire together, wire together x

18

What is long-term potentiation?

When useful synapses are strengthened - increased plasticity

19

What 4 things happen to strengthen a synapse?

- more receptors
- receptor function improved
- more transmitter made
- more transmitter released

20

How are memories formed?

Secondary messengers from activation of metabotropic receptors enhance long-term potentiation process.

21

Discuss spontaneous potentials

Some excitable cells fire spontaneous bursts of action potentials, due to unstable membrane potential - in the heart for example.